Differences in Albuminuria Between Hispanics and Whites: An Evaluation by Genetic Ancestry and Country of Origin The Multi-Ethnic Study of Atherosclerosis Carmen A. Peralta, MD, MAS; Yongmei Li, PhD; Christina Wassel, PhD; Shweta Choudhry, PhD; Walter Palmas, MD; Michael F. Seldin, MD; Neil Risch, PhD; David Siscovick, MD, MPH; Donna Arnett, PhD, MSPH; Bruce Psaty, MD, PhD; Michael G. Shlipak, MD, MPH Background—Reports show higher prevalence of albuminuria among Hispanics compared with whites. Differences by country of origin or genetic background are unknown. Methods and Results—In Multi-Ethnic Study of Atherosclerosis, we studied the associations of both genetic ancestry and country of origin with albumin to creatinine ratio among 1417 Hispanic versus white participants using multivariable linear regression and back transforming beta coefficients into relative difference (%RD, 95% CI). Percentage European, Native American, and African ancestry components for Hispanics were estimated using genetic admixture analysis. The proportions of European, Native American, and African genetic ancestry differed significantly by country of origin (P0.0001); Mexican/Central Americans had the highest Native American (4113%), Puerto Ricans had the highest European (6115%), and Dominicans had the highest African (3921%) ancestry. Hispanic ethnicity was associated with higher albumin/creatinine ratio compared with whites, but the association varied with the country of origin (adjusted P interaction=0.04). Mexican/Central Americans and Dominicans had higher albumin/creatinine ratio compared with whites after adjustment (RD 19%, 2% to 40% and RD 27%, 1% to 61%), but not Puerto Ricans (RD 8%, -12% to 34%). Higher Native American ancestry was associated with higher albuminuria after age and sex adjustment among all Hispanics (RD 11%, 1% to 21%) but was attenuated after further adjustment. Higher European ancestry was independently associated with lower albumin/creatinine ratio among Puerto Ricans (-21%, -34% to -6%) but not among Mexican/Central Americans and Dominicans. Conclusions—Hispanics are a heterogeneous group with varying genetic ancestry. Risks of albuminuria differ across the country of origin groups. These differences may be due, in part, to differences in genetic ancestral components. (Circ Cardiovasc Genet. 2010;3:240-247.) Key Words: genetics  kidney  albuminuria  ancestry H ispanics have a higher incidence of end-stage renal disease compared with whites in the United States, 1 despite reports that Hispanics have lower prevalence of chronic kidney disease (CKD). 2,3 Although this discrepancy may be explained by Hispanics having faster rates of pro- gression from CKD to end-stage renal disease, 4 it may also be complicated by the use of different definitions to describe “Hispanics.” For example, CKD prevalence estimates have focused on Mexican Americans 3 whereas end-stage renal disease estimates have included a wider group of Hispanics. 1 Because Hispanic subgroups in the United States differ culturally, socially, and perhaps genetically, 5,6 categorization of Hispanics into 1 homogeneous group could lead to spurious inferences that may not generalize. Editorial see p 223 Clinical Perspective on p 247 Differences between Hispanics and whites have also been reported for albuminuria, a marker of early kidney damage, and a known risk factor for CKD progression. 7 Studies from Received October 7, 2009; accepted April 20, 2010. From the Department of Medicine (C.A.P., S.C., M.G.S.), University of California San Francisco; General Internal Medicine (C.A.P., Y.L., M.G.S.), San Francisco VA Medical Center, San Francisco, Calif; Department of Family and Preventive Medicine (C.W.), University of California, San Diego, Calif; Department of Medicine (W.P.), Columbia University, New York, NY; Human Genetics and Departments of Biochemistry and Molecular Medicine, and Medicine (M.F.S.), University of California, Davis; Institute of Human Genetics and Department of Epidemiology and Biostatistics (N.R.), University of California, San Francisco, Calif; Departments of Medicine and Epidemiology and Cardiovascular Health Research Unit (D.S.), University of Washington, Seattle, Wash; Department of Epidemiology (D.A.), University of Alabama, Birmingham, Ala; Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology, and Health Services (B.P.), University of Washington; and Center for Health Studies (B.P.), Group Health, Seattle, Wash. Guest Editor for this article was Judith S. Hochman, MD. Correspondence to Carmen A. Peralta, MD, MAS, 4150 Clement St, 111A1, San Francisco, CA 94121. E-mail CarmenAlicia.Peralta@ucsf.edu © 2010 American Heart Association, Inc. Circ Cardiovasc Genet is available at http://circgenetics.ahajournals.org DOI: 10.1161/CIRCGENETICS.109.914499 240 Downloaded from http://ahajournals.org by on August 16, 2022